The underlying objective of this proposal is to understand, at the molecular level, a problem of developmental nature. In bacteriophage T4, several kinds of mutant are now available, which, at some stage of virus assembly, alter the fidelity of the normal capsid length- determining mechanism. Rather precisely defined classes of abnormally short (petit) capsids as well as abnormally long (giant) capsids are produced by these mutants. By precise genetic mapping these mutations have been shown to be located in gene 23 which codes for the major structural protein of the T4 capsid. The objective of the program is to understand, at the molecular level, the mechanism by which capsid length is determined. It will be approached by determining the amino acid sequences of the normal and the mutant gene-23 proteins of T4. Comparison of these sequences is expected to give some insight into the way in which the fidelity of the length determining mechanism has been altered, which, in turn, should lead to some understanding of the nature of genetic control of form.